Arsenic in drinking water and the prevalence of respiratory effects in West Bengal, India

et al. 2004

IJERPH

This study conducted in Bangladesh reports the relationship of clinical complications with nutritional status and the prevalence of leukopenia among arsenic exposed patients living in the rural villages. A total of 115 exposed individuals diagnosed as arsenicosis patients were randomly selected from four known arsenic endemic villages, and age-matched 120 unexposed subjects were enrolled in the study program. The duration of arsenic exposure in about 37% of the patients was at least 10 yrs, while the population mean and range were 7.6 ± 5.2 yrs, and 1 -25 yrs, respectively. The mean arsenic concentrations in the drinking water for the exposed and unexposed (control) population were 218.1 µg/L and 11.3 µg/L, respectively. The spot urine sample of the arsenicosis patients contained an average of 234.6 µg/L arsenic. Although very few patients showed elevated WBC count, 16% had leukopenia (below normal count), and the whole population had significantly low WBC count than the control subjects. Prevalences of neutropenia and lymphocytosis were observed in patients with chronic exposure to high levels of arsenic in water. The body mass index was found to be lower than 18.5, the cut-off point for malnutrition (underweight), in about 28% of the arsenicosis cases compared to 15% of the controls. The monthly income and total calorie consumption per day showed the patients were underprivileged than the controls. Arsenical symptoms and complications were more severe in the nutritionally vulnerable (underweight) patients than the overweight ones. Also, the incidences of leukopenia and anaemia were more common in the female patients who were underweight. The findings of this research demonstrate that the poor nutritional status of patients increases the complications of chronic arsenic toxicity; suggest the possibility of other sources of arsenic contamination different from drinking water in the study area; and establish a higher prevalence of leukopenia and lymphocytosis in arsenicosis patients.

Section: Number Of Patients With Clinical Symptomssupporting

confidence: 58%

Association of Clinical Complications with Nutritional Status and the Prevalence of Leukopenia among Arsenic Patients in Bangladesh

Islam

Nabi

et al. 2004

IJERPH

“…Although many reports relied on the concentrations of arsenic in drinking water (Mazumder et al, 1998;Hopenhayn-Rich et al, 1998;Kurttio et al, 1998;Tondel et al, 1999;Bhattacharya et al, 2002;Anawar et al, 2002;Frisbie et al, 2002) as the surrogate of human exposure, potential individual consumption of water and additional exposure through food had been neglected. The biological dose indicators would neither give any information on the absolute intake level nor on the relative relevance of different arsenic sources, especially the importance of water versus food arsenic, which would be important in establishing risk assessment and in determining the priority for mitigation (Watanabe et al, 2004).…”

Section: Arsenic Intake In Human Body From Cooked Rice and Drinking Wmentioning

confidence: 99%

Influence of cooking method on arsenic retention in cooked rice related to dietary exposure

Hasegawa

Science of The Total Environment

et al. 2006

104

Arsenic concentration in raw rice is not only the determinant in actual dietary exposure. Though there have been many reports on arsenic content in raw rice and different tissues of rice plant, little is known about arsenic content retained in cooked rice after being cooked following the traditional cooking methods employed by the people of arsenic epidemic areas. A field level experiment was conducted in Bangladesh to investigate the influence of cooking methods on arsenic retention in cooked rice. Rice samples were collected directly from a severely arsenic affected area and also from an unaffected area, to compare the results. Rice was cooked according to the traditional methods employed by the population of subjected areas. Arsenic concentrations were 0.40±0.03 and 0.58±0.12 mg/kg in parboiled rice of arsenic affected area, cooked with excess water and 1.35±0.04 and 1.59±0.07 mg/kg in gruel for BRRI dhan28 and BRRI hybrid dhan1, respectively. In non-parboiled rice, arsenic concentrations were 0.39±0.04 and 0.44±0.03 mg/kg in rice cooked with excess water and 1.62±0.07 and 1.74±0.05 mg/kg in gruel for BRRI dhan28 and BRRI hybrid dhan1, respectively. Total arsenic content in rice, cooked with limited water (therefore gruel was absorbed completely by rice) were 0.89±0.07 and 1.08±0.06 mg/kg (parboiled) and 0.75±0.04 and 1.09±0.06 mg/kg (non-parboiled) for BRRI dhan28 and BRRI hybrid dhan1, respectively. Water used for cooking rice contained 0.13 and 0.01 mg of As/l for contaminated and non-contaminated areas, respectively. Arsenic concentrations in cooked parboiled and non-parboiled rice and gruel of non-contaminated area were significantly lower (p<0.01) than that of contaminated area. The results imply that cooking of arsenic contaminated rice with arsenic contaminated water increases its concentration in cooked rice.

Toxicology and Applied Pharmacology

“…Previous research of the effects of chronic exposure to iAs has focused primarily on its carcinogenic potential. However, chronic exposures to iAs from the environment or in occupational settings have also been linked to non-carcinogenic diseases, including peripheral vascular disease, cardiovascular and cerebrovascular diseases Chen et al, 1996;Chiou et al, 1997;Engel et al, 1994;Thomas and Goyer, 1995;Tseng et al, 1995;Tseng et al, 1997), hypertension , goiter (Chang et al, 1991), hepatomegaly (Santra et al, 1999), respiratory system dysfunction (Mazumder et al, 2000), nervous system dysfunction (Bencko et al, 1977;Chisolm Jr. and Thomas, 1983;Masahiko and Hideyasu, 1973), and diabetes mellitus (Lai et al, 1994;Rahman et al, 1998;Rahman et al, 1999;Tseng et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Examination of the effects of arsenic on glucose homeostasis in cell culture and animal studies: Development of a mouse model for arsenic-induced diabetes

Paul

Hernández-Zavala

Walton

et al. 2007

125

Previous epidemiologic studies found increased prevalences of type 2 diabetes mellitus in populations exposed to high levels of inorganic arsenic (iAs) in drinking water. Although results of epidemiologic studies in low-exposure areas or occupational settings have been inconclusive, laboratory research has shown that exposures to iAs can produce effects that are consistent with type 2 diabetes. The current paper reviews the results of laboratory studies that examined the effects of iAs on glucose metabolism and describes new experiments in which the diabetogenic effects of iAs exposure were reproduced in a mouse model. Here, weanling male C57BL/6 mice drank deionized water with or without the addition of arsenite (25 or 50 ppm As) for 8 weeks. Intraperitoneal glucose tolerance tests revealed impaired glucose tolerance in mice exposed to 50 ppm As, but not to 25 ppm As. Exposure to 25 and 50 ppm As in drinking-water resulted in proportional increases in the concentration of iAs and its metabolites in the liver and in organs targeted by type 2 diabetes, including pancreas, skeletal muscle and adipose tissue. Dimethylarsenic was the predominant form of As in the tissues of mice in both 25 and 50 ppm groups. Notably, the average concentration of total speciated arsenic in livers from mice in the 50 ppm group was comparable to the highest concentration of total arsenic reported in the livers of Bangladeshi residents who had consumed water with an order of magnitude lower level of iAs. These data suggest that mice are less susceptible than humans to the diabetogenic effects of chronic exposure to iAs due to a more efficient clearance of iAs or its metabolites from target tissues.